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目的:研究抗毒补心胶囊对阿霉素诱导所致心肌损伤大鼠的心肌保护作用并探讨其机制。方法:SD大鼠60只,随机分成6组,除空白组外,均采用每周1次ip阿霉素3 mg.kg-1共6周,制备慢性心肌损伤模型,治疗组同时分别给予抗毒补心胶囊低、中、高剂量(0.4,0.8,1.6 g.kg-1),阳性对照组给予复方丹参片(0.45 g.kg-1)。检测心肌损伤大鼠左心射血分数(LVEF)、左室缩短分数(FS)及血浆脑钠素(BNP)、心肌谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,并进行心肌病理检查。结果:经阿霉素诱导慢性心肌损伤后,大鼠血浆BNP水平升高,心肌组织MDA含量增高,GSH-Px,SOD活性降低(P<0.01);抗毒补心胶囊治疗组的LVEF和FS均较模型组高,血浆BNP水平下降,且心肌MDA含量降低,GSH-Px,SOD活性升高(P<0.05)。结论:抗毒补心胶囊具有抗氧化作用,对阿霉素所引起的慢性心肌损伤有保护作用。
Objective: To study the protective effects of Kangdu Buxin Capsule on doxorubicin-induced myocardial injury in rats and its mechanism. Methods: Sixty Sprague-Dawley rats were randomly divided into 6 groups. Except for the blank group, rats were treated with 3 mg.kg-1 of doxorubicin 3 mg.kg-1 once a week for 6 weeks to prepare chronic myocardial injury model. Dubu Xin Capsule low, medium and high doses (0.4,0.8,1.6 g.kg-1), the positive control group given compound Danshen tablets (0.45 g.kg-1). The levels of left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS), plasma BNP, GSH-Px and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, and myocardial pathological examination. Results: After adriamycin-induced chronic myocardial injury, plasma BNP level increased, MDA content increased, and the activity of GSH-Px and SOD decreased (P <0.01); LVEF and FS Compared with the model group, plasma BNP level decreased, MDA content decreased and GSH-Px and SOD activities increased (P <0.05). Conclusion: Kangdu Buxin Capsule has anti-oxidant effect and protects against chronic myocardial injury caused by doxorubicin.